Degenerative spine disease is a major cause of chronic disability in the adult working population
and a common reason for referral to an MR imaging center. Spinal degeneration is a normal part of
aging, and neck and back pain are one of life's most common infirmities. There are many potential
sources of pain, and finding the specific cause is often a confounding problem for both patient and
doctor. Pain can originate from bone, joints, ligaments, muscles, nerves and intervertebral disks, as
well as other paravertebral tissues. The landmark article by Mixter and Barr in 1934
on the ruptured
intervertebral disk provided an anatomic basis for selected cases of back pain and neurologic
dysfunction. Most neck and back pain responds to conservative therapy, but if the pain is unrelenting,
severe, or associated with a radiculopathy or myelopathy, imaging is indicated to look for a treatable
cause.

EXAMINATION TECHNIQUE

In the evaluation of degenerative spine disease, multiple anatomic sites need to be imaged,
including the intervertebral disk, spinal canal, spinal cord, nerve roots, neuroforamina, facet joints,
and the soft tissues within and surrounding the spine. Many pulse sequences are available, and
specific protocols vary among different MR sites. There is general agreement that the spine needs
to be imaged in at least two planes, and surface coils are used almost exclusively. In the cervical and
thoracic regions a T2-weighted sequence is mandatory to assess damage to the spinal cord. Thin
sections are required to visualize the neuroforamina, and pulse sequences must be tailored to
counteract CSF flow and physiologic motion. The imaging requirements for the lumbar spine are less
strenuous because the anatomical parts are larger. Most protocols include a T1-weighted sequence
and some type of T2-weighted sequence to give a myelographic effect.
Fast spin-echo (FSE)
techniques allow enormous time savings, and if available, they have replaced conventional spin-echo
for T2-weighted imaging of the spine. Three-dimensional gradient-echo (GRE) methods can achieve
slice thicknesses less than one millimeter, an advantage for displaying cervical neuroforamina.

In the postoperative spine, gadolinium injection with T1-weighted imaging is essential to evaluate
enhancing lesions. Fat-suppression is helpful to eliminate competing fat signal from bone marrow and
other soft tissues.

INTERVERTEBRAL DISK DISEASE

Pathophysiology

The normal intervertebral disk consists of the nucleus pulposus surrounded by the anulus fibrosus.
Both the anulus and the nucleus are composed of collagen and proteoglycans (chondroitin-6-sulfate,
keratan sulfate, hyaluronic acid, and chondroitin-4-sulfate). The nucleus contains relatively more
proteoglycans to give it a looser gelatinous texture. It blends in with the surrounding anulus without
clear anatomic demarcation. The anulus has more collagen, and the collagen becomes progressively
more compact and tougher at the periphery. The outer anulus is attached to the adjacent vertebral
bodies at the site of the fused epiphyseal ring by Sharpey's fibers and to the anterior and posterior
longitudinal ligaments. Normal disks are well hydrated, the nucleus containing 80 to 85% water and
the anulus about 80%.
Together with the cartilaginous end plates of the adjacent vertebral bodies,
the intervertebral disk forms a disk complex that gives structural integrity to the interspace and
cushions the mechanical forces applied to the spine.

With aging, certain biochemical and structural changes occur in the intervertebral disks. There
is an increase in the ratio of keratan sulfate to chondroitin sulfate, and the proteoglycans lose their
close association with the disk collagen. The disk also loses its water-binding capacity and the water
content decreases down to 70%. These changes are reflected by a 6% decrease in MR signal intensity
over a span of 79 years.
The vertebral end plates also becomes thinner and more hyalinized. This
degree of disk degeneration is considered a normal part of aging.

With more advanced degeneration, dense disorganized fibrous tissue replaces the normal
fibrocartilaginous structure of the nucleus pulposus, leaving no distinction between the nucleus and
anulus fibrosus. Development of anular tears weakens the anulus and allows nucleus to protrude into
the defect. Tears that extend through the outer anulus induce ingrowth of granulation tissue and
accelerate the degenerative process. Advanced degeneration can lead to gas formation or
calcification within the disk. Also, fissures develop in the cartilaginous end plates, and regenerating
chondrocytes and granulation tissue form in the area.

Desiccation - loss of disk water

Disk bulge - circumferential enlargement of
the disk contour in a symmetric fashion

Protrusion - a bulging disk that is eccentric to
one side but < 3 mm beyond vertebral
margin

Patients with lumbar disk disease can
present with back pain or a radicular pain
syndrome. The classic sciatic syndrome consists of stiffness in the back and pain radiating down to
the thighs, calves and feet, associated with paresthesias, weakness, and reflex changes. The pain from
intervertebral disk disease is exacerbated by coughing, sneezing, or physical activity. Pain is usually
worse when sitting, and with straightening or elevating the leg. Disk herniations occur most often
at the lower lumbar levels - 90% at L4-5 and L5-S1, 7% at L3-4, and remaining 3% at the upper 2
levels.

Disk Degeneration

One of the earliest signs of disk degeneration is loss of water content or desiccation, most
noticeable in the nucleus pulposus. MR can detect early disk degeneration because, as the disks lose
water, the MR signal decreases on gradient-echo and T2-weighted images. With more advanced
degeneration, the disk collapses and gas may form within the disk. Calcification is not uncommon
in chronic degenerative disk disease.

As a consequence of intervertebral disk degeneration, normal axial loading on the spine stretches
and lengthens the anular fibers, resulting in rounded, symmetric bulging of the disk beyond the
margins of the vertebral body. A bulging disk encroaches on the ventral spinal canal and inferior
portions of the neuroforamina but does not displace or impinge the nerve roots. The combination of
sagittal and axial views provides excellent visualization of the relationships of the disk to the spinal
canal and neural foramina. When there is a generalized paucity of epidural fat, producing an MR
"myelogram" with gradient-echo or T2-weighted images is helpful to show the relationship of the disk
with the thecal sac.

In an anatomic and MR study of cadaveric spines, Yu and colleagues
found three types of anular
tears in degenerated disks. Concentric tears (Type I) are caused by rupture of the short transverse
fibers connecting the lamellae of the anulus, and were seen as crescentic or oval spaces filled with
fluid or mucoid material. In radial tears (Type II)
the longitudinal fibers are disrupted through all
layers of the anulus, from the surface of the anulus
to the nucleus. Transverse tears (Type III) result
from rupture of Sharpey's fibers near their
attachments with the ring apophysis, and are
imaged as irregular fluid-filled cavities at the
periphery of the anulus.

Anular tears are depicted on MR scans as
small focal areas of hyperintensity on sagittal T2-
weighted images.
Transverse tears are located at
the periphery of the anulus adjacent to the
vertebral margins. Radial tears tend to be more
irregular and obliquely oriented. High-signal-
intensity zones on T2-weighted MR images are commonly seen along the posterior margin of
degenerated disks in asymptomatic patients. The high-signal-intensity does not imply acute disk
disruption, and no association with trauma has been proven.
They probably represent small
transverse or concentric tears in the outer annular fibers

Complete disruption of the anulus exposes the nuclear material to the epidural tissues, inducing
a focal inflammatory reaction. Vascular granulation tissue forms and grows into the disk through the
anular tear. Enhanced MR images will detect more anular tears than T1 or T2-weighted images -
mostly radial tears, but also a few transverse tears.

Degeneration of the intervertebral disk has secondary effects on the adjacent vertebral end plates
and bone marrow. As discussed earlier in the section on pathophysiology, fissures develop in the
cartilaginous end plates in concert with disk degeneration. Vascular granulation tissue grows into
the fissures and induces an edematous reaction and vascular congestion in the adjacent bone marrow.
Modic's group
has classified the bone marrow changes according to the signal intensity on MR
images. This first reaction of bone marrow edema and vascular congestion, called Type 1 change,
is hypointense on T1 and hyperintense on T2-weighted images. Type 1 change routinely enhances
with gadolinium and can simulate osteomyelitis. With time, the bone marrow converts to a
predominantly fatty marrow (Type 2 change). Longitudinal studies have shown this fatty marrow
replacement to be stable over a 2-3 year period. Type 2 change is hyperintense on T1 and isointense
to hypointense on T2-weighted images, the exact signal intensity dependent on the degree of T2-weighting. Chronic disk disease leads to dense sclerosis of the vertebral end plates and adjacent
vertebral bodies (Type 3 change). Conversion from Type 1 to Type 3 change generally requires a few
years time. Type 3 change is reflected on the MR images as hypointensity on both T1 and T2-weighted images.

Disk Protrusion/Herniation

Any radial tear of the anulus is a potential site for herniation of the nucleus pulposus. On the
sagittal view, dissection of nucleus pulposus through radial tears of the anulus is clearly depicted.
Defects in the anulus with disk extending posteriorly are indicative of protrusion/herniation. In the
sagittal plane, a herniated disk has an hourglass appearance along the posterior disk margin, which
is described as a "squeezed toothpaste" effect. Axial scans show either asymmetry of the posterior
disk margin or a soft-tissue mass displacing adjacent intraspinal structures.

Most disk herniations occur in a posterolateral direction into the spinal canal because the tough
posterior longitudinal ligament is thicker and tougher in the middle and resists posterior extension
near the midline. A herniated disk usually impinges on the nerve root as it courses inferiorly toward
the foramen at the next lower level. For example, an L4-L5 herniated disk impinges on the L5 root.
The L4 root is likely unaffected unless there is lateral and cephalad migration of a free fragment into
the neural foramen.

The neural foramina are visualized on parasagittal images of the lumbar spine, and disk herniation
can be detected by obliteration of foraminal fat. Nevertheless, axial MR is better for visualizing
lateral disk herniations. Lateral disks compress the nerve root within the foramen or just beyond its
lateral margin distal to the nerve root sheath.

In the lumbar region, Ross's group
found marked enhancement, distinct from epidural venous
plexus, surrounding disk herniations. Histology disclosed peridiskal scar tissue similar to the epidural
scar observed in postoperative patients. The depth of penetration of the scar depends on how long
the disk fragment has been in the epidural space. The vascular scar tissue is a part of the body's repair
mechanism to resorb and remove the offending disk material. Over time, the entire disk fragment may
be resorbed.

Free Fragments

When an extruded disk loses its attachment to the parent disk, it becomes a free fragment or
sequestration. If the disk fragment is near an interspace, sometimes it can be difficult to discern
whether or not a pedicle of attachment remains. Free fragments can migrate some distance cephalad
or rostral to the disk space, and it is important to alert the surgeon to their precise location. Rarely,
a disk fragment may rupture through the thecal sac into the intradural compartment.

Most sequestered disks are higher signal than their disk of origin on T2-weighted images. The
cause for this is unclear, but it may be due to increased water from granulation tissue, immune
response, and inflammation.
Chronic disk herniations tend to be hypointense due to loss of water
content.

Subligamentous disk fragments are contained by the posterior longitudinal ligament (PLL).
Schellinger and colleagues
reviewed the anatomy of the PLL and anterior epidural space. Most
contained disk fragments lateralize to either side of the anterior epidural space. An equal number
migrate superiorly and inferiorly. The PLL has a high collagen content and is hypointense on MR.
It can be seen as a thick dark line covering a contained herniated disk, usually seen best on sagittal
images. The posterior margin of contained disk fragments usually maintain a smooth contour.

Non-contained disk fragments have gone through the PLL. Either interruption or absence of the
peripheral dark line suggests disruption of the PLL.
Once through the PLL, the disk fragments are
not bounded by any membranes, and they tend to have more irregular contours.

Effect on Nerve Roots

The most direct effect on the nerve root is from compression by the herniated disk, but the disk
need not compress the nerve root directly to cause radicular pain. Fragments of nucleus pulposus
within the epidural space induce a focal inflammatory reaction that can secondarily irritate the
adjacent nerve root.

In a study by Jinkins,
nerve root enhancement was observed in 5% of patients scanned for back
or leg pain. Of that group, 70% had disk protrusion and a radicular pain pattern in the distribution
of the enhancing root. The other 30% without protruding disk had multiple enhancing roots,
suggesting an idiopathic low-grade inflammation. Lane's group
reported that multilevel nerve root
enhancement, especially when continuous from the root sleeve cephalad toward the conus, is often
asymptomatic and not associated with any nerve root compression. The continuous enhancement
probably represents radicular veins.

Significance and Natural History

The determination of clinically significant disk disease is an important radiologic and clinical
decision because the possible consequences of back surgery are not insignificant. Identification of
nerve root compression or severe effacement of the thecal sac, especially ventrolaterally, that
correlates with radicular pain or a muscle weakness pattern supports the operative approach when
conservative medical therapy has failed. But beyond that, things are less certain. Annular tears and
focal disk protrusions are frequently found in asymptomatic populations. The annuloligamentous
complex is richly innervated by the recurrent meningeal nerve. Annular tears involving this complex
may be a source of diskogenic pain due to exposure of the nerve endings to the acid metabolites of
the protruding nucleus pulposus.

Jensen and his group
detected MR signs of intervertebral disk disease, consisting of bulge,
protrusion, or extrusion, in 64% of asymptomatic adult subjects. Moreover, disk herniation does not
relate directly to back pain or a radicular pain syndrome. In a study by Boden and colleagues,
lumbar disk herniations were found in 28% of asymptomatic patients over 40 years of age.

Furthermore, patients with symptomatic disk herniations don't necessarily require surgery.
Bozzao and colleagues
followed 69 patients with herniated lumbar disks for 6 to 15 months while
they were under conservatively medical therapy. On follow-up MR imaging, 63% showed a
reduction in size of their herniated disk of more than 30%, 48% showed a reduction of more than
70%, and only 8% got worse or enlarged. Larger herniations were more likely to decrease, which
they attributed to more vascularity or granulation tissue. The excellent depiction of abnormal
morphology by MR imaging provides an opportunity to investigate further the natural history of
intervertebral disk disease.

Cervical Spine

Cervical disk disease occurs most commonly at the levels of C5-6 and C6-7. A central disk
herniation will most likely cause a myelopathy due to cord compression, along with neck pain and
stiffness. If the disk extends laterally to compress nerve roots, the pain may radiate to the shoulder,
arm, or hand.

A sagittal T1 study shows the margins of the spinal cord with respect to other structures within
the spinal canal. Subtle scalloping of the cord may be present due to encroachment posteriorly by
ligamentum flavum hypertrophy or anteriorly by disk or spondylosis. Because disk, ligaments, and
bone have low or absent signal on T1-weighted images, it may not be possible to differentiate these
structures from one another. The increased contrast between the CSF containing thecal sac and
adjacent structures on T2-weighted FSE or GRE images improves visualization of extradural lesions
that impinge on the thecal sac.

Degeneration of the intervertebral disk is accompanied by loss of water content and therefore
signal intensity on MR images. Loss of disk signal is not a necessary prerequisite for disk herniation.
On T1 images a herniated disk generally has the same signal characteristics as the parent disk and is
seen as an extrusion of disk material into the spinal canal.
Herniated disks can be midline or lateral,
and it is important to clearly identify the location of the disk fragment for surgical planning.
Midline
extradural lesions can be identified on sagittal views by effacement of the thecal sac or cord, but when
eccentric they may be seen better on the axial views. Normal signal intensity in the neural foramina
may be diminished due to displacement of either epidural veins or foraminal fat.

High-signal above and below a herniated disk is frequently seen and most likely represents flow
enhancement in engorged epidural veins containing slowly flowing blood. On parasagittal scans, flow
enhancement in these veins may be the best indicator of an epidural abnormality when a central
component is absent.

Indentation or compression of the cord is common with larger disks and is seen best on T2-weighted or gradient-echo sagittal images. When either herniated disks or osteophytes impinge on
the spinal cord, cord injury can result, which points out the importance of prompt, accurate diagnosis
and definitive therapy. As with any contusion, cord edema and swelling develop that may be seen as
focal high-signal intensity on T2-weighted scans. There is also disruption of the blood-cord barrier,
so enhancement may be observed with Gadolinium.

Thoracic Spine

Symptomatic thoracic disks are uncommon, accounting for about 1% of all
disk herniations. The rib cage, small intervertebral disks, and coronal
orientation of the facets joints all contribute to limited mobility of the
thoracic spine, and consequently, a lower risk of disk herniation. The most
common level is T11-T12, where the spine is relatively less rigid. Sagittal
T2-weighted FSE sequences are excellent for displaying indentation of ventral
thecal sac and impingement of the spinal cord by thoracic disks. Axial images
help delineate lateralization to either side. Disk morphology is similar
to the cervical region. Calcification is more common in thoracic disk fragments
and parent disks than in cervical or lumbar region.

SPONDYLOSIS

Spondylosis can take the form of marginal end plate osteophytes, enlarged uncinate processes,
or facet arthrosis. Degenerative joint disease itself, along with associated inflammatory reaction, can
cause pain, or the symptoms can be derived from the osteophytes compressing neural structures. It
is important to distinguish spondylosis from disk disease for therapeutic planning.

Vertebral Body Osteophytes

Marginal osteophytes form around the periphery of the vertebral body end plates of the lumbar
spine. The larger ones generally project anteriorly or directly lateral and do not compress neural
structures. Posterior and posterolateral osteophytes are more likely to cause problems.

Osteophytes are hypointense on all pulse sequences. Identification of central osteophytes requires
gradient-echo or T2-weighted images to achieve good contrast between the osteophytes and the
hyperintense CSF within the thecal sac. On T1-weighted scans, osteophytes may be silhouetted by
the low-signal CSF Posterior ridging osteophytes produce broad ventral impressions on the thecal
sac. In the cervical spine, if the posterior bony ridges are large, they can cause repeated trauma to
the spinal cord with neck motion, eventually resulting in cord deformity, atrophy, and a myelopathy.

In the lumbar region, osteophytes encroaching on neural foramina are contrasted nicely by foraminal fat on T1-weighted scans. The lumbar neural foramen has the shape of an inverted teardrop,
with the nerve root positioned in the superior aspect of the foramen. Fortunately, small osteophytes
project first into the inferior aspect of the foramen and are unlikely to compress the nerve root until
they get quite large.

Unco-Vertebral and Facet Joint Arthrosis

Some degree of spondylosis is invariably associated with degenerative disk disease. Decrease in
height of the intervertebral disk places more stress on the facet joints and unco-vertebral joints,
leading to degenerative joint disease. Moreover, with the loss of structural strength at the disk level,
exaggerated motion occurs at these joints, accelerating the degenerative changes and placing stress
upon the posterior supporting ligaments as well.

The unco-vertebral joints (uncinate processes) are unique to the cervical spine. With
degeneration, osteophytes develop at these joints and project into the lateral spinal canal and
foramina. Symptoms are caused by impingement of nerve roots as they exit the foramina.

Not all back pain or sciatica is due to intervertebral disk disease. Degeneration of the facet joint
can cause a facet arthrosis syndrome, consisting of back pain aggravated by rest and relieved by
repeated gentle motion.
Facet joint hypertrophy, along with osteophyte formation along the
posterior lateral margins of the vertebral body, can
encroach upon the lateral recesses of the spinal canal
and the neural foramina. Compression of the existing
nerve roots results in a radicular pain syndrome, called
the lateral recess syndrome.

MR shows the changes of facet sclerosis and the
osteophytes but not the cartilage degeneration.
Accurate assessment of mild foraminal narrowing
requires high-quality images and is aided by careful
patient positioning so that both foramina are sectioned
together on the axial images. MR performs better in
cases of moderate to severe foraminal disease.
Volume acquisition methods with oblique image
reformation are helpful for evaluating patients with
cervical radiculopathy.

Synovial Cysts

Juxtaarticular synovial cysts are associated with facet arthropathy, generally of fairly severe
degree. They consist of a fibrous wall, often with a distinct synovial lining, and a cystic center that
may or may not communicate with the facet joint. They are found most frequently at L4-5, the more
mobile segment of the lumbar spine. Synovial cysts can compress the dorsal nerve roots and cause
radicular symptoms.

On MR scans, synovial cysts appears as smooth, well-defined extradural masses in the
posterolateral spinal canal. They are positioned adjacent to a facet joint and dorsal to or merges with
a thickened ligamentum flavum. The cystic center has a highly variable MR signal pattern due to the
spectrum of fluid components (serous, mucinous, or gelatinous), air, and hemorrhagic components.
The hypointense perimeter reflects the fibrous capsule with calcium or hemosiderin from chronic
hemorrhage, as well as the companion joint capsule and adjacent ligaments.
The fibrous capsule
may enhance with gadolinium. The combination of proton-density and T2-weighted axial images are
best for detecting and delineating these lesions.

SPINAL STENOSIS

Spinal stenosis refers to constriction of the canals and various foramina of the spine. If
sufficiently severe, the stenosis can compress neural structures within the spine and cause neurological
symptoms. Spinal stenosis can involve the spinal canal, the lateral recesses, or the neuroforamina.
Spondylosis and spinal stenosis are commonly associated with intervertebral disk disease, particularly
in patients over 50, and they are significant sources of neck and back pain and radiculopathy.
Overlooking the patho-anatomic changes of spinal stenosis is an important cause of the failed back
surgery syndrome after diskectomy.

Spinal stenosis is due to congenitally short pedicles, or it may be acquired as a result of combined
facet hypertrophy, degenerated bulging disk, and hypertrophy of the ligamentum flavum. Congenital
spinal stenosis can be idiopathic or associated with a developmental disorder, such as achondroplasia,
hypochondroplasia, Morquio's mucopoly-saccharidosis, and Down's syndrome. Spondylolisthesis,
trauma, and surgical fusion are other causes of spinal stenosis.

Lumbar Spine

Congenital spinal stenosis is often asymptomatic until middle age, when secondary degenerative
changes develop. The acquired type is a disease of primarily adult men with moderate to severe
degenerative spine disease. The syndrome of
neurogenic or spinal claudication includes
bilateral lower extremity pain, numbness, and
weakness that is poorly localized and usually
associated with low back pain. The
symptoms are worse with standing or walking
and relieved when the patient lies down.

Spinal stenosis is graphically displayed in
the sagittal plane by gradient-echo or T2-
weighted pulse sequences. The hyperintense
thecal sac is effaced anteriorly by the bulging
disk and posteriorly by the ligamentum
flavum, resulting in an hourglass
configuration. Acquired spinal stenosis is
usually associated with moderate to severe
multilevel disk degeneration, consisting of
loss of normal signal, disk space narrowing,
and intradiskal calcification or air. The
calcification and air can be difficult to discern within severely desiccated disks. On axial views the
constricted canal often has a triangular or trefoil shape due to encroachment on the posterolateral
aspects of the canal by hypertrophied facets.

Since compression of the nerve roots within the thecal sac causes the symptoms, assessment of
the ratio of CSF to nerve roots is important to make the diagnosis of spinal stenosis. With
progressive stenosis, the amount of CSF progressively diminishes and the nerve roots become
crowded together. Constriction at the level of stenosis prevents the normal superior and inferior
movement of the nerve roots with flexion and extension, resulting in a redundant serpiginous root
pattern above and below the stenosis. Nerve root enhancement may also be seen, due to either
breakdown of the blood-nerve barrier from mechanical injury, inflammatory response, and Wallerian
degeneration/regeneration of axons, or engorgement of intrathecal veins and perineural vascular
plexus. As a result of epidural compression, prominent enhancement of retrovertebral venous plexus
is common.

Cervical Spine

When bulging disks, spondylosis, and ligamentum flavum hypertrophy progress to constrict the
spinal canal and cord, a spinal stenosis develops. These changes are depicted on sagittal gradient-echo or T2-weighted images as hourglass narrowing of the thecal sac, usually involving multiple levels
in the mid- and lower cervical region. In patients with a congenitally borderline or narrow canal,
relatively mild degenerative changes are sufficient to cause spinal stenosis. On T1-weighted scans,
canal stenosis results in scalloping of the normally smooth dorsal and ventral margins of the cord.
As learned from myelography, the degree of canal stenosis and cord scalloping shown on the images
is greater when the neck is in a hyperextended position, due to buckling of the ligamentum flava.
Imaging in a neutral position may show less severe stenosis. Nonetheless, the hyperextended view
illustrates what happens to the cord with acute hyperextension. The spinal cord is more susceptible
to traumatic injury in patients with spinal stenosis.

SPONDYLOLISTHESIS

Spondylolysis refers to a cleft or break in the pars interarticularis of the vertebra. It is found in
about 6% of adults, mostly in males, 93-95% occur at L5, and most are bilateral. The etiology is
uncertain, but the current theory is that it represents a stress fracture from repeated trauma to the
spine.
The pars defect is demonstrated best in parasagittal images and is easier to see if the bone
has a generous component of marrow or if soft tissue is interposed between the bone fragments.
With subluxation, there is often a step-off at the pars defect. On axial views, the key observation is
a horizontal line (an extra joint) between adjacent facets joints on consecutive images.

Spondylolisthesis refers to forward displacement of one vertebra over another, usually of the fifth
lumbar over the body of the sacrum,
or of the fourth lumbar over the fifth.
Spondylolisthesis is graded according
to how far the vertebral body moves
forward on the one below (Grade 1 =
25%, Grade 2 = 50%, Grade 3 =
75%). There are two types of
spondylolisthesis, isthmic (open-arch
type), associated with spondylolysis,
and degenerative (closed-arch type).

With isthmic spondylolisthesis,
the pars defect divides the vertebra
into an anterior part (vertebral body,
pedicles, transverse processes, and
superior articular facet) and a
posterior part (inferior facet, laminae, and spinous process). The anterior part slips forward, leaving
the posterior part behind. As a result, the spinal canal elongates in its anteroposterior dimension, so
that spinal canal stenosis is uncommon with isthmic spondylolisthesis. Grade I spondylolisthesis is
often asymptomatic, but with progressive anterior subluxation, the intervertebral disk and the
posterior-superior aspect of the vertebral body below encroach on the superior portion of the neural
foramen.
The foramen is also elongated in a horizontal direction and may have a bilobed
configuration. Exuberant fibrocartilage at the pars pseudarthrosis can further compromise the neural
foramen and cause nerve root compression.

Degenerative spondylolisthesis occurs in an older age group, usually over 60 years old, and it is
more common in women at the level of L4-L5. It develops when there are severe degenerative
changes and excess motion of the facet joints. Subluxation at the facet joints allows forward or
posterior movement of one vertebra over another. A degenerative spondylolisthesis narrows the
spinal canal, and symptoms of spinal stenosis are common. Hypertrophic facet arthrosis is a frequent
cause of foraminal narrowing.

The sagittal plane is best for
displaying the abnormal anatomy of
spondylo-listhesis, T2-weighted images
for the canal and T1-weighted images for
the pars interarticularis and neural
foramina. The sagittal view clearly
shows the degree of subluxation and the
relationship of the intervertebral disk to
the adjacent vertebral bodies and the
spinal canal. Parasagittal images are
good for showing encroachment on the
foramina by disk or hypertrophic bone.
Loss of the normal fat signal cushioning
the nerve root is a sign for significant
foraminal stenosis.

Ulmer and colleagues
proposed the "wide canal sign" to distinguish between isthmic and
degenerative spondylolisthesis. Using a midline sagittal section, they noted that the sagittal canal
ratio (maximum anteroposterior diameter at any level divided by the diameter of the canal at L1) did
not exceed 1.25 in normal controls and in subjects with degenerative spondylolisthesis. In patients
with spondylolysis, the measurement always exceeded 1.25.

POSTOPERATIVE SPINE

In the early postoperative period, interpretation of the MR images is extremely difficult. The
presence of fat graft, hematoma, gas, and inflammation complicates the observed signal intensities.
Moreover, recurrent disk and epidural scar exhibit similar topographical and signal characteristics.
After about one month, the acute postoperative changes resolve, making it easier to distinguish scar
from disk. As before surgery, recurrent disk is often in continuity with the parent disk. Discontinuity
in the anulus fibrosus is not entirely reliable because it can result from the surgical incision as well as
from disk rupture. Unless the disk material has become separated as a free fragment or sequestration,
it remains similar in signal characteristics to the parent disk on both T1- and T2-weighted images.
In general, herniated disks are relatively well-defined and, in some cases, have a hypointense rim.

On the other hand, epidural scar has poorly defined margins and is either isointense or hypointense
on short TR/TE sequences compared to the adjacent disk. With more T2-weighting, scar generally
increases in signal, but to a lesser degree many months or years after surgery. In addition, if the soft-tissue abnormality can be followed posteriorly along the lateral margin of the spinal canal to the
region of the laminectomy, it is probably scar. Retraction of the thecal sac to the side of the soft
tissue is another sign favoring postoperative scar.

Gadolinium should be used routinely in the postoperative back because it is a valuable aid for
differentiating the various postoperative tissues. Epidural scar enhances to a much greater degree
on MR than on contrast-enhanced CT. The enhancing scar clearly identifies nerve roots trapped
within the scar and outlines any retained or recurrent disk fragments. A disk fragment induces a local
inflammatory reaction, and vascular granulation tissue often forms about its perimeter. As a result,
the perimeter of a herniated disk may enhance with gadolinium, but the central part will not, thus
distinguishing it from epidural scar.